Every two years the Canadian Obesity Network holds its National Obesity Summit – the only national obesity meeting in Canada covering all aspects of obesity – from basic and population science to prevention and health promotion to clinical management and health policy.
Anyone who has been to one of the past four Summits has experienced the cross-disciplinary networking and breaking down of silos (the Network takes networking very seriously).
Of all the scientific meetings I go to around the world, none has quite the informal and personal feel of the Canadian Obesity Summit – despite all differences in interests and backgrounds, everyone who attends is part of the same community – working on different pieces of the puzzle that only makes sense when it all fits together in the end.
The 5th Canadian Obesity Summit will be held at the Banff Springs Hotel in Banff National Park, a UNESCO World Heritage Site, located in the heart of the Canadian Rockies (which in itself should make it worth attending the summit), April 25-29, 2017.
Yesterday, the call went out for abstracts and workshops – the latter an opportunity for a wide range of special interest groups to meet and discuss their findings (the last Summit featured over 20 separate workshops – perhaps a tad too many, which is why the program committee will be far more selective this time around).
So here is what the program committee is looking for:
- Basic science – cellular, molecular, physiological or neuronal related aspects of obesity
- Epidemiology – epidemiological techniques/methods to address obesity related questions in populations studies
- Prevention of obesity and health promotion interventions – research targeting different populations, settings, and intervention levels (e.g. community-based, school, workplace, health systems, and policy)
- Weight bias and weight-based discrimination – including prevalence studies as well as interventions to reduce weight bias and weight-based discrimination; both qualitative and quantitative studies
- Pregnancy and maternal health – studies across clinical, health services and population health themes
- Childhood and adolescent obesity – research conducted with children and or adolescents and reports on the correlates, causes and consequences of pediatric obesity as well as interventions for treatment and prevention.
- Obesity in adults and older adults – prevalence studies and interventions to address obesity in these populations
- Health services and policy research – reaserch addressing issues related to obesity management services which idenitfy the most effective ways to organize, manage, finance, and deliver high quality are, reduce medical errors or improve patient safety
- Bariatric surgery – issues that are relevant to metabolic or weight loss surgery
- Clinical management – clinical management of overweight and obesity across the life span (infants through to older adults) including interventions for prevention and treatment of obesity and weight-related comorbidities
- Rehabilitation – investigations that explore opportunities for engagement in meaningful and health-building occupations for people with obesity
- Diversity – studies that are relevant to diverse or underrepresented populations
- eHealth/mHealth – research that incorporates social media, internet and/or mobile devices in prevention and treatment
- Cancer – research relevant to obesity and cancer
…..and of course anything else related to obesity.
Deadline for submission is October 24, 2016
To submit an abstract or workshop – click here
For more information on the 5th Canadian Obesity Summit – click here
For sponsorship opportunities – click here
Looking forward to seeing you in Banff next year!
Now a study by Peter Nordström and colleagues, published in JAMA Internal Medicine, reports that a higher BMI in identical twins is associated with a greater risk for type 2 diabetes but not myocardial infarction or death.
The researchers looked at data from 4,046 monzygous twin pairs with discordant BMIs (difference >0.01 units) from the nationwide Swedish twin registry.
During a mean follow-up of 12 years, the rate of myocardial infarcts and deaths were similar in the twins with lower BMI compared to their higher BMI co-twin (5.0% vs. 5.2% and 13.6% vs. 15.6%, respectively).
This lack of difference remained true even when the researchers compared the extremes of BMI discordance and only considered twins with BMI greater than 30.
In contrast, both higher BMI and greater increase in BMI since 30 years before baseline was associated with greater risk of incident diabetes.
Given that diabetes is such a powerful risk factor for cardiovascular disease, one can only wonder why this did not translate into a higher cardiovascular risk in the higher weight twins.
One possible explanation, offered by the authors is that cardiovascular risk may have been well managed in these individuals thus minimizing any increased risk due to diabetes (or other BMI associated risk factors such as dyslipidemia or hypertension).
Indeed, it would probably have required a far larger group of twins (or much longer follow-up) to fully rule out higher cardiovascular risk in these twins.
Let us also not forget that BMI is a rather lousy measure of overall cardiovascular risk.
Thus, which the study is certainly compatible with the (genetics-independant?) role of higher BMI in the risk for diabetes, it certainly should not be interpreted as demonstrating that this increased risk in benign in terms of cardiovascular disease.
In all of my interactions with people who believe that the obesity epidemic is vastly overblown and that the links between excess body fat are imagined, I often hear the argument that obesity cannot “cause” [chose your health problem here] because “normal-weight” people can have [same health problem] too!
This is a rather naive argument, pretty much along the lines of, “Tobacco cannot cause lung cancer because non-smokers can get lung cancer too, or alcohol cannot cause liver cirrhosis because teetotalers get cirrhosis too”.
Or, “Drunk driving cannot cause road accidents, because non-drunk drivers get into accidents too”.
Or, “Flu vaccines don’t work, because vaccinated people get the flu too”.
I could go on….
What is missing in this perspective, is a very basic understanding of multiple cause and effect, as well as a fundamental understandings of probability and risk.
Firstly, almost all medical conditions can have more than one cause. Thus, although most lung cancer is by far attributable to smoking, it is also seen with exposure to asbestos, other environmental toxins, and of course sporadic mutagenesis.
Similarly, there are a multitude of reasons why someone may get liver cirrhosis, but, at least in Western societies, alcohol consumption is by far the number one cause of this problem.
And yes, some vaccinated people do catch the flu, but most vaccinated people don’t and when they do, it turns out to be less severe than it would have been without the vaccine.
So, just because “normal-weight” people can also have hypertension, diabetes, fatty liver disease, sleep apnea, osteoarthritis, gastroesophageal reflux, urinary incontinence, plantar fasciitis, and a host of other conditions, does not “prove” that excess weight does not also “cause” all of these conditions.
Yes, skinny people can have sleep apnea too but the overwhelmingly vast majority of sleep apnea is seen in people with excess weight – the same goes for virtually every obesity related health problem.
The other argument I often hear is that obesity cannot be the cause of [chose your health problem here] because not all people with obesity have [same health problem].
This argument is likewise stupid!
The fact that not every smoker dies of lung cancer, in no way “proves” that smoking does not cause cancer.
The fact that not everyone who regularly drinks a lot of alcohol gets a cirrhotic liver, does not disprove the link between alcohol and cirrhosis.
This is where we need to understand the basic concept of risk and probability.
When a certain factor (e.g. excess body fat) increases the risk of a certain condition, it does not mean that everyone exposed to that factor ends up with the condition. It just means that the risk for that condition is vastly higher.
Now let’s add a further level of complexity to the concept of risk, because, as we know, body fat is not body fat is not body fat is not body fat!
Whether or not my body fat actually causes any health problem, depends on a wide range of factors ranging from my underlying genetic predisposition (e.g. for diabetes, hypertension, etc.), my fat location (subcutaneous vs. ectopic), the cellular structure of my fat (hypertrophic vs. hyperplastic), fat-tissue inflammation, and probably countless other factors.
Add to this, that risk for obesity related conditions can be substantially modified by other factors including physical fitness, healthy diets, positive body image, good mental health – it is easy to understand why defining “sick” and “healthy” simply based on a measurement (direct or indirect) of body fat makes no sense.
Thus, we need to ensure that the medical term “obesity” is not used to label everyone above a certain (arbitrary) BMI cutoff.
Rather, we should reserve the medical term “obesity” only for the condition where excess or abnormal body fat directly impairs the health of a given individual (the actual WHO definition of obesity!).
Someone with the exact same amount of body fat (or even more), who does not experience any health impairment should not be referred to as having “obesity” – that person is just “fat” (a word that really needs to be destigmatised!).
Personally, I couldn’t care less about how “fat” anyone is. Only when “fat” becomes “obesity” does it become a medical issue.
Yesterday, I posted about the significant weight loss seen with the glucagon-like peptide 1 (GLP-1) analogue semaglutide in patients with type 2 diabetes, a finding that holds promise for the use of this agent for obesity treatment.
Now, Juan Frias and colleagues, in a paper published in Lancet Diabetes & Endocrinology, present data showing an additive weight-loss effect of combining the GLP-1 analogue exanatide with the SGLT2 inhibitor dapagliflozin in patients with type 2 diabetes.
The DURATION-8 trial randomised 695 patients with type 2 diabetes to a combination of once-weekly GLP-1 agonist exenatide (Bydureon(R)) and the SGLT-2 inhibitor dapagliflozin (Farxiga(R)) vs. either drug as monotherapy for 28 weeks.
While the combination was superior in all diabetes-related end-points to monotherapy with either substance, I was particularly interested in also seeing superior weight loss with the combination.
Thus, overall patients on dual therapy with exenatide and dapagliflozin lost 3.41 kg vs. 1.54 kg and 2.19 kg on monotherapy, respectively.
However, participants with a baseline A1c between 8% and 9% appeared to experience a greater, more additive weight loss, with participants treated with both dapagliflozin and exenatide experiencing a mean weight loss of 4.5 kg weight reduction, compared to 1.9 kg with exenatide and 2.2 kg with dapagliflozin.
Importantly perhaps, adverse events occurred with approximately equal frequency in each group, suggesting that the combination was as well tolerated as either substance alone.
Again, it is important to note that this was a diabetes study in patients with diabetes and not a study designed to test the efficacy of this drug combination for weight loss, a study design that would have also included diet and exercise recommendations to maximise the effect of this combination.
As I have argued before, given the complexity of the body’s defence mechanisms against weight-loss, the future probably lies in the use of combination treatments for obesity (not unlike the widespread use of combination therapies for diabetes or hypertension).
Thus, it is certainly of interest to see that combining two drugs with different modes of action does indeed produce additive effects on body weight.
Disclaimer: I have received speaking honoraria from Astra Zeneca, the maker of dapagliflozin
Anyone who follows these pages is aware of the fact that we desperately lack better medical treatments for obesity.
Last year, Health Canada approved the glucagon-like peptide 1 (GLP-1) analogue liraglutide (Saxenda(R)) for obesity treatment, which although effective and generally well-tolerated, has to be administered by daily injections.
Now, the results of the SUSTAIN-6 trial, published in the New England Journal of Medicine, show that the once weekly injection of the GLP-1 analogue semaglutide, not only decreases cardiovascular events, but also significantly lowers body weight, a promising finding for future obesity treatment with this drug.
The SUSTAIN 6 trial randomised 3297 patients with type 2 diabetes to once-weekly semaglutide (0.5 mg or 1.0 mg) or placebo for 104 weeks.
At baseline, 2735 of the patients (83.0%) had established cardiovascular disease, chronic kidney disease, or both.
The primary outcome (MACE) occurred in 108 of 1648 patients (6.6%) in the semaglutide group and in 146 of 1649 patients (8.9%) in the placebo group (hazard ratio, 0.74).
Nonfatal myocardial infarction occurred in 2.9% of the patients receiving semaglutide and in 3.9% of those receiving placebo (hazard ratio, 0.74); nonfatal stroke occurred in 1.6% and 2.7%, (hazard ratio, 0.61).
While average body weight at week 104 remained stable in the placebo group, it decreased by 3.6 kg in the semaglutide 0.5 mg group and and 4.9 kg in the semaglutide 1.0 mg group.
While this may not seem spectacular, it is important to remember that weight loss is notoriously difficult in patients with type 2 diabetes and that this was a diabetes and not an obesity trial, in which case participants would have also been counselled to change their diet and activity levels to achieve weight loss.
Thus, one can only speculate on what the differences in body weight would have been had the participants been actually trying to lose weight.
That said, it was perhaps surprising to note that fewer serious adverse events occurred in the semaglutide group, although more patients discontinued treatment because of adverse events, mainly gastrointestinal.
It will be interesting to see how well semaglutide fares in studies in which this treatment is assessed for the obesity indication, which will hopefully bring us closer to a once-weekly medication for obesity.
In the meantime, once-daily liraglutide 3.0 mg is certainly a welcome addition to medical management of obesity, but clearly there is more to come in terms of harnessing GLP-1 for obesity management.
Disclaimer: I have received consulting and speaking honoraria from Novo Nordisk, the makers of liraglutide and semaglutide